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Jie, Q.

Publications and source records attributed to Jie, Q..

3 recordsLinked to original sources

Asymmetric subspecies-selection of an NLR-TF immune module and reconstruction of broad-spectrum disease resistance in rice

Artificial selection has greatly shaped crop agronomic traits; however, the mechanistic basis of immunity selection has remained elusive. This study identifies a new rice NLR XA48 and its downstream transcription factor OsVOZ1, which confer bacterial blight resistance. XA48 perceives an ancient pathogen effector, XopG, to activates effector-triggered immunity (ETI). The XA48-OsVOZ1 module has undergone subspecies-specific selection. Xa48 is retained in indica but functionally lost in japonica rice. OsVOZ1 has also diverged into two haplotypes, indica kept both OsVOZ1A/S alleles that match XA48; while japonica only inherited OsVOZ1A that greatly decreases yield when Xa48 is reintroduced into japonica, mechanistically explaining the Xa48 loss in japonica. We resurrected wild rice broad-spectrum resistance by stacking XA48-mediated ETI with XA21-mediated pattern-triggered immunity (PTI). Thus, our study reveals that the asymmetric selection of an NLR-TF module shapes both disease resistance and reproduction, and provides a paradigm for breeding crops by harnessing the immunity of wild relatives.

genetics↗

COMT inhibitor tolcapone represses the migration and invasion of trophoblast and results in preeclampsia-like phenotypes in mice

Pregnancy in young-onset Parkinsons disease (YOPD) is rare; however, medication for this condition is critical for maternal and fetal health. Tolcapone is an effective antiparkinsonian drug. However, its safety studies on mothers and fetuses are limited. In this study, we aimed to investigate the effects of tolcapone on the mother and the developing fetus during different stages of gestation. Tolcapone was administered to pregnant mice at a dose of 60 (H-Tol) or 30 mg/kg/day (L-Tol) during early or mid-gestation. We observed that tolcapone administration during early gestation causes abortion and delays fetal development in a dose-dependent manner. During mid-gestation tolcapone barely caused embryo lethality; however, the mice developed preeclampsia-like phenotypes, including maternal hypertension, proteinuria, and fetal growth restriction. Histomorphological analysis of placentas from tolcapone treated mice revealed abnormalities in the trophoblast layer and the impaired trophoblast invasion in the decidua. Mechanistically, we revealed that tolcapone inhibits the invasion and migration of trophoblasts in vitro, with changes in the protein expression of Snail, Twist, and E-cadherin. In conclusion, tolcapone caused embryo lethality and growth restriction during early gestation, whereas it caused preeclampsia-like phenotypes in mice with defective trophoblast invasion in mid-gestation. Collectively, our study provides novel insights into the effects of tolcapone on pregnancy.

pharmacology and toxicology↗

Specific Deletion of Axin1 Leads to Activation of β-Catenin/BMP Signaling Resulting in Fibular Hemimelia Phenotype in Mice

Axin1 and Axin2 are key regulators of canonical Wnt signaling pathway. The roles of Axin1 and Axin2 in skeletal development and in disease development have not been fully defined. Here, we reported that Axin1 and Axin2 are essential for lower limb development. Specific deletion of Axin1 in limb mesenchymal cells leads to fibular hemimelia (FH)-like phenotype, associated with tarsal coalition. Further studies demonstrated that FH disease is associated with additional defects resembling to the proximal femoral focal deficiency (PFFD) in Axin1/Axin2 double knockout (KO) mice. We then provided in vivo evidence showing that Axin1 controls limb development through both canonical {beta}-catenin and BMP signaling pathways. We demonstrated that inhibition of {beta}-catenin or BMP signaling could significantly reverse the FH phenotype in mice. Together, our findings revealed that integration of Wnt and BMP signaling by Axin1 is required for lower limb development. Defects in Axin1 and Axin2 signaling could lead to the development of FH disease.

developmental biology↗